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The studies, done independently by researchers at Columbia and Harvard, involved genetically engineered mice that could make abnormal human tau proteins, predominantly in the entorhinal (pronounced en-toh-RYE-nal) cortex, a sliver of tissue behind the ears, toward the middle of the brain, where cells first start dying in Alzheimer’s disease. As expected, tau showed up there. And, as also expected, entorhinal cortex cells in the mice started dying, filled with tangled, spaghettilike strands of tau.Over the next two years, the cell death and destruction spread outward to other cells along the same network. Since those other cells could not make human tau, the only way they could get the protein was by transmission from nerve cell to nerve cell.And that, said Dr. Samuel E. Gandy, associate director of the Alzheimer’s Disease Research Center at Mount Sinai School of Medicine in New York, was “very unexpected, very intriguing.â€ÂAlthough the studies were in mice, researchers say they expect that the same phenomenon occurs in humans because the mice had a human tau gene and the progressive wave of cell death matched what they see in people with Alzheimer’s disease.
That may be the single gayest thing I have ever read on this board. Or the old one.
There are very few problems that cannot be solved with a good taint punching.
Fascinating. I want to study neuroscience.